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Pathological Processes > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Cell injury

A

All cells have effective mechanisms to deal with mild changes in environmental conditions.

More severe changes in environment lead to cell adaptation, injury or cell death.

Degree of injury depends on: -

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2
Q

What causes cell injury?

A

Hypoxia

Toxins

Physical agents - Direct trauma

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3
Q

Hypoxia

A

Hypoxia versus ischaemia
Causes of hypoxia:
hypoxaemia hypoxia - arterial content of oxygen is low (occurs with reduced inspired pO2 at altitude and reduced absorption secondary to lung disease

anaemia hypoxia - decreased ability of Hb to carry oxygen (anaemia and CO poisoning)

Ischaemic hypoxia - interruption to blood supply (blockage of a vessel and heart failure)

Histiocytic hypoxia - inability to utilise oxygen in cells due to disabled OxP enzymes (cyanide poisoning)

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4
Q

Immune system damaging damaging body’s cells

A

Hypersensitivity reactions -host tissue is injured secondary to an overly vigorous
immune reaction, e.g., urticaria (= hives)

Autoimmune reactions -immune system fails to distinguish self from non-self

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5
Q

Toxins

A

Glucose and salt in hypertonic solutions, high conc of O2, poisons, pollutants, insecticides, herbicides, asbestos, alcohol, Narcotic drugs, medicines

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6
Q

Which cell components are most susceptible to injury

A
  1. Cell membranes - Plasma membrane and Organellar membranes
  2. Nucleus - DNA
  3. Proteins - Structural (Enzymes)
  4. Mitochondria - disruption of Oxidative phosphorylation
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7
Q

What is happening at molecular level at hypoxia

A

Blockage in capillary means cells further along the capillary dont receive oxygenated blood

Mitochondria cant do ETC so no OxP

ATP pump doesn’t work well

So you get:
— sodium pump doesn’t work as well as no ATP, so high Na+ conc, causes influx of Ca2+ + water and flux of K+ ions - all this leads to cellular swelling, ER welling and loss of cell integrity

Calcium conc increase in cells also causes major problems as it activates some fo the protease and nucleases

— Increase in glycolysis for anaerobic respiration could lead to build up of lactate and lactic acid which decreases pH which can cause clumping of nuclear chromatin in the nucleus

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8
Q

What about prolonged hypoxia

A

At some point the damage can become irreversible

Can lead to complete membrane permeability

Ca flows in

Can’t activate any enzymes leading to detrimental effects

By activation of ATPase (causes decreased ATP), phospholipids (causes decreased phospholipids), protease (causes disruption of PM) and endonucleases (causes nuclear chromatin damage

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9
Q

Cell injury with causes other than hypoxia

A

Sequence of events for other insults may be different but as the cell has a limited responses to injury, outcome often similar.

Other forms of injury might attack different key structures, e.g., extreme cold (e.g., frostbite) damages membranes initially.

Free radicals also damage membranes primarily.

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10
Q

What are free radicals?

A

These are reactive oxygen (and nitrogen) species

Single unpaired electron in an outer orbit

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11
Q

3 radicals are of particular biological significance in cells

A

OH

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12
Q

Free radicals are formed by

A

UV light - Air pollution - Ionising radioation - Smoking - Metabolism - Inflammation

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13
Q

When are free radicals produced

A
  1. Normal metabolic reactions: e.g., oxidative phosphorylation
  2. Inflammation: oxidative burst of neutrophils
  3. Radiation: H20 —> 0H.
  4. Contact with unbound metals within the body: iron (by Fenton reaction) and copper
    Free radical damage occurs in haemachromatosis and Wilson
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14
Q

How do free radicals injure cells

A

If the number of free radicals overwhelms the anti-oxidant system = oxidative imbalance

Most important target are lipids in cell membrane

Cause lipid periodisation, this leads to generation of further free radicals —> auto catalytic chain reaction

Also oxidise proteins, carbohydrates and DNA, These molecules become bent out of shape, broken or cross-linked

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15
Q

How does the body control free radicals

A
  1. Anti-oxidant scavengers: donate electrons to the free radical
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16
Q

How else can the cell protect itself against injury

A

Heat shock proteins - In cell injur

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17
Q

Mechanisms of intracellular accumulations

A

1) abnormal metabolism
2) alterations in protein folding and transport
3) deficiency of critical enzymes
4) inability to degrade phagocytosed particles

Seen when metabolic processes become deranged

Often occur with sublethalor chronic injury

Can be reversible

Can be harmless or toxic

They can derive from the -

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18
Q

What kind of things can accumulate in cells?

A

1) water and electrolytes
2) lipids
3) Carbs
4) Proteins
5) pigments

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19
Q

When does fluid accumulate in cells

A

Hydropic swelling

Occurs when energy supplies are cut off e.g. hypoxia

Indicates severe cellular distress

Na+ and water flood into cell

Particular problem in the brain

20
Q

When might lipid accumulate in the cell

A

Stratus is (accumulation of TGs)

Often see in liver (the major organs of fat metabolism)

If mild - then mostly asymptomatic
Causes - alcohol, DM, obesity and Toxins (e.g. carbon tetrachloride)

Cholesterol - Cannot be broken down and is insoluble

Can only be eliminated through the liver

Excess stored in cell ion vesicles

Accumulates in smooth muscle cells and macrophages in ATS plaques = foam cells

Present in macrophages in skin and tendons of people with hereditary hyperlipidaemias

21
Q

Accumulation of proteins in cells

A

Seen as eosinophilic droplets or aggregations in the cytoplasm

ALD - mallory’s hyaline (damaged keratin filaments present in hepatocytes)

Alpha1-antitrypsin deficiency - liver produces incorrectly folded alpha1-antitrypsin protein (a protease inhibitor)

Cannot be packed by ER, accumulates in the ER and is not secreted

Leads to systemic deficiency - protease in the lung act unchecked leading to emphysema

22
Q

Accumulation of pigment in cells

A

Carbon/ coal dust/ soot - urban air pollutant
Inhaled and phagocytosed by alveolar macrophages

Anthracosis and blackened peribronchial lymph nodes

Usually harmless, unless in large amounts = fibrosis and emphysema = coal workers pneumoconiosis

Tattooing - pigments pricked into skin

Phagocytosed by macrophages in dermis and remains there, some pigment will reach draining lymph nodes

23
Q

Accumulation of endogenous pigments

A

Haemosiderin - iron storage molecule - derived from Hb, yellow/brown

24
Q

What is hereditary haemochromatosis

A

Genetically inherited disorder -results in increased intestinal absorption of dietary iron

Iron is deposited in skin, liver, pancreas, heart and endocrine organs - often associated with scarring in liver (cirrhosis) and pancreas.

Symptoms include liver damage, heart dysfunction and multiple endocrine failures, especially of the pancreas.

Was called

25
Q

Jaundice

A

Accumulation of bilirubin - bright yellow

Breakdown of heme, stacks of broken porphyria rings

Formed in all cells of body (cytochromes contain heme) but must be eliminated by bile

Taken from tissues by albumin to liver, conjugated with bilirubin and excreted in bile

If bile flow is obstructed or overwhelmed, bilirubin in blood rises and jaundice follow

Depositied in tissues extracellularly or in macrophages

26
Q

When membranes are leaky and what leaks out

A

Yes, and they can have both local and systemic effects:

27
Q

Calcification of tissues

A

Abnormal deposition of calcium salts within tissues.
Can be localised (dystrophic) or generalised (metastatic)
Dystrophic: - Much more common that metastatic
Occurs in an area of dying tissue, atherosclerotic plaques, aging or damaged heart valves, in
tuberculus lymph nodes, some malignancies

Why does dystrophic calcification occur?
No abnormality in calcium metabolism, or serum calcium or phosphate concentrations

Local change/disturbance favours nucleation of hydroxyapatite crystals

Can cause organ dysfunction, e.g., atherosclerosis, calcified heart valves

Why does metastatic calcification occur?

28
Q

Hypercalcamia

A

Increased secretion of parathyroid hormone (PTH) resulting in bone resorption:

29
Q

Cell death definitions

A

Oncosis - cell death with swelling, the spectrum of changes that occur in injured cells prior to death

Necrosis: in a living organism the morphologic changes that occur after a cell has been dead some
time - Seen after 12-24 hours

30
Q

Types of necrosis

A

Two main types -

31
Q

Coagulative necrosis

A

Denaturation of proteins dominates over release of active proteases.

Cellular architecture is somewhat preserved, “ghost outline

32
Q

Liquefactive necrosis

A

Enzyme degradation is substantially greater than denaturation.
Leads to enzymatic digestion (liquefaction) of tissues. Cells just fall apart - left with pink debris

33
Q

Caseous necrosis

A

Contains amorphous (structureless) debris. (c.f. ghost outline in coagulative necrosis).

Particularly associated with infections, especially tuberculosis.

34
Q

Fat necrosis

A

Destruction in the adipose tissue - seen in individuals with acute pancreatitis e.g. alcoholics

35
Q

Gangrene, infarction and infarct

A

Gangrene= necrosis visible to the naked eye - An appearance of necrosis

Infarction= necrosis caused by reduction in arterial blood flow - A cause of necrosis - Can result in gangrene

Infarct= an area of necrotic tissue which is the result of loss of arterial blood supply - An area ischaemic necrosis

36
Q

Wet and dry gangrene

A

Dry gangrene = necrosis modified by exposure to air (coagulative necrosis)

Wet gangrene = necrosis modified by infection (liquefactive necrosis)

Gas gangrene - wet gangrene where the infection is with anaerobic bacteria that produce gas

37
Q

Common causes of infarction

A

Thrombosis - blockage occurs at original site

Embolism - block that travels in blood vessels comes to narrow tissues and gets stuck

38
Q

White infarcts

A

= anaemic infarcts
Solid organs - occlusion of an end artery

Often wedge shaped

Coagulative necrosis

39
Q

Why are some infarcts red

A

= haemorrhagic infarct

Loose tissue

Dual blood supply

Numerous anastomoses

Prior congestion

Raised venous pressure

Re-perfusion

40
Q

Consequence of infarction

A

Can range form None to death

Depends on:

41
Q

Ischaemia-repercussion injury

A

Paradoxically, if blood flow is returned to a damaged but not yet necrotic tissue, damage
sustained can be worse than if blood flow hadn

42
Q

Apoptosis

A

cell death with shrinkage, induced by a regulated intracellular program where a cell
acti

43
Q

Physiological and pathological apoptosis?

A

When does apoptosis occur physiologically?

  1. In order to maintain a steady state
  2. Hormone-controlled involution
  3. Embryogenesis - stain for apoptotic cells in the developing paw of a foetal mouse. - Sculpting

When does apoptosis occur pathologically?
Cytotoxic T cell killing of virus-infected or neoplastic cells
When cells are damaged, particularly with damaged DNA
Graft versus host disease

44
Q

3 stages of apoptosis

A

Initiation
Execution
Degradation & phagocytosis

Initiation and execution - Triggered by two mechanisms

45
Q

Can cells live forever

A

As cells age they accumulate damage to cellular constituents and DNA

Pathological Processes (14 decks)

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